Endothelial cells regulate astrocyte to neural progenitor cell trans-differentiation in a mouse model of stroke.
Wenlu LiEmiri T MandevilleVioleta Durán-LaforetNorito FukudaZhanyang YuYi ZhengAaron HeldJi-Hyun ParkTakafumi NakanoMasayoshi TanakaJingfei ShiElga EspositoWanting NiuChanghong XingKazuhide HayakawaIgnacio LizasoainKlaus van LeyenXun-Ming JiBrian J WaingerMaría Angeles MoroEng H LoPublished in: Nature communications (2022)
The concept of the neurovascular unit emphasizes the importance of cell-cell signaling between neural, glial, and vascular compartments. In neurogenesis, for example, brain endothelial cells play a key role by supplying trophic support to neural progenitors. Here, we describe a surprising phenomenon where brain endothelial cells may release trans-differentiation signals that convert astrocytes into neural progenitor cells in male mice after stroke. After oxygen-glucose deprivation, brain endothelial cells release microvesicles containing pro-neural factor Ascl1 that enter into astrocytes to induce their trans-differentiation into neural progenitors. In mouse models of focal cerebral ischemia, Ascl1 is upregulated in endothelium prior to astrocytic conversion into neural progenitor cells. Injecting brain endothelial-derived microvesicles amplifies the process of astrocyte trans-differentiation. Endothelial-specific overexpression of Ascl1 increases the local conversion of astrocytes into neural progenitors and improves behavioral recovery. Our findings describe an unexpected vascular-regulated mechanism of neuroplasticity that may open up therapeutic opportunities for improving outcomes after stroke.
Keyphrases
- endothelial cells
- cerebral ischemia
- mouse model
- resting state
- subarachnoid hemorrhage
- white matter
- high glucose
- single cell
- nitric oxide
- functional connectivity
- type diabetes
- cell proliferation
- brain injury
- cell therapy
- multiple sclerosis
- adipose tissue
- vascular endothelial growth factor
- metabolic syndrome
- mesenchymal stem cells
- transcription factor
- blood glucose
- insulin resistance